Clinical microbiology and hospital infection control: AmpC beta-lactamase: practice question

A Microbiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Microbiology · Clinical microbiology and hospital infection control: AmpC beta-lactamase

Sample item

Enterobacter cloacae from a patient treated with ceftriaxone for five days, initially susceptible, is now resistant to ceftriaxone and cefoxitin. Adding clavulanate does not restore susceptibility. Which mechanism is most likely?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Derepressed chromosomal AmpC beta-lactamase

Enterobacter carries an inducible chromosomal AmpC enzyme, and therapy with third-generation cephalosporins selects derepressed mutants that hydrolyse cephalosporins and cefoxitin, and are not inhibited by clavulanate. ESBLs spare cefoxitin and are inhibited by clavulanate.

Option by option

  • A. Metallo-beta-lactamase NDM carbapenemase production

    NDM would also confer carbapenem resistance, which is not described.

  • B. Acquisition of the mecA gene encoding PBP2a

    mecA is found in staphylococci, not in Enterobacter.

  • C. Plasmid-borne TEM-type extended-spectrum enzyme

    ESBLs are inhibited by clavulanate and do not hydrolyse cefoxitin.

  • D. Derepressed chromosomal AmpC beta-lactamase (correct)

    Correct. AmpC hyperproduction gives cefoxitin and ceftriaxone resistance with no clavulanate effect.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Microbiology question

What is the answer to this Microbiology question?

The best answer is D, Derepressed chromosomal AmpC beta-lactamase. Enterobacter carries an inducible chromosomal AmpC enzyme, and therapy with third-generation cephalosporins selects derepressed mutants that hydrolyse cephalosporins and cefoxitin, and are not inhibited by clavulanate.

Why is "Metallo-beta-lactamase NDM carbapenemase production" not the answer?

NDM would also confer carbapenem resistance, which is not described.

Why is "Acquisition of the mecA gene encoding PBP2a" not the answer?

mecA is found in staphylococci, not in Enterobacter.

Why is "Plasmid-borne TEM-type extended-spectrum enzyme" not the answer?

ESBLs are inhibited by clavulanate and do not hydrolyse cefoxitin.

What concept does this question test?

It tests Clinical microbiology and hospital infection control: AmpC beta-lactamase in Microbiology. ESBLs spare cefoxitin and are inhibited by clavulanate.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Clinical microbiology and hospital infection control: AmpC beta-lactamase?

Make a one-line identity card for each organism: shape and stain, defining test, toxin, disease and drug. Then use the flashcards and the other Microbiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.